1. Description of the problem

Therapeutic hypothermia is used as a neuroprotective measure following cardiac arrest. High-level evidence exists for this indication, and it is the standard of care at most tertiary medical centers worldwide. Its use is experimental/unproven in the management of traumatic brain injury, spinal cord injury, refractory status epilepticus, and ischemic stroke.

Therapeutic hypothermia is also a treatment option for refractory intracranial hypertension with good evidence for efficacy but few outcome data to support overall benefit vs. harm. Finally, it is used for neonatal hypoxic-ischemic brain injury, an indication beyond the current scope of discussion.

Patients who have suffered hypoxic-ischemic brain injury and remain comatose should be considered eligible recipients for therapeutic hypothermia. Comatose is generally defined as not able to be aroused to the point of following commands.

Hypothermia should be initiated immediately in patients with return of spontaneous circulation after cardiac arrest who have not awakened.

2. Emergency Management

Post-cardiac arrest with suspected hypoxic-ischemic brain injury:

Management points not to be missed

Successful cardiac resuscitation with return of spontaneous circulation (pressor support is OK)

3. Diagnosis

Considerations

A patient resuscitated after cardiac arrest, who remains comatose, does not mandate any specific neurologic testing prior to inducing hypothermia. In the real-world setting, patients are often 'found down' and a head CT is obtained to rule out intracranial hemorrhage (either as the primary event causing arrest or from cranial trauma due to falling, etc). Cervical spine plain films and/or CT are obtained to look for cervical injury. EKG and cardiac enzymes should be obtained immediately, as in any patient with suspected acute coronary syndrome.

Laboratory and toxicologic evaluation should also proceed as indicated by the clinical situation to evaluate for electrolyte abnormalities, hypoglycemia, and drug or alcohol intoxication. EEG monitoring, if available, can be used to monitor for seizures during the cooling phase of the hypothermia protocol and during rewarming. There is currently no indication for acute EEG monitoring in the initial phase of treatment (ambulance or emergency room).

Prognostication hinges on neurologic examination after rewarming and in the days to follow. This should be guided by a neurologist. EEG monitoring is emerging as a useful prognostic tool. However, somatosensory evoked potentials are currently the only test with adequate predictive value to be relied upon in the clinical setting.

Special considerations for nursing and allied health professionals.

Hypothermia should be induced immediately in comatose survivors of cardiac arrest; all care providers should realize the urgency of delivering neuroprotective therapy as soon as possible. Positioning injuries and decubitus ulcers may be more likely in the hypothermic patient who is peripherally vasoconstricted. Frost-bite injuries can occur from surface cooling devices or ice packs. Finally, respiratory therapists should ask the physician whether to temperature-correct the arterial blood gas samples or not (i.e. pH-stat vs. alpha-stat management), since this will affect ventilatory management.